Citation : Sevket O, Adem D, Ali Ekber A, et al Rivaroxaban in Venous Pulmonary Thromboembolism. The first experience of new oral anticoagulant. JJ Pulmono 2019; 5(1): 040.

Case ReportA Case With Neurogenic Pulmonary Edema

Sevket Ozkaya1*,Tugce Uzar2, Melisa Aslan3, Ozgur Celik4,Adem Dirican5,Zehra Yavuz6 and Pankina Ekaterina7

1Department of Pulmonary Medicine, MD, Pulmonologist, Asoc. Prof., Bahcesehir University,Faculty of Medicine,Istanbul, Turkey

2 Medical Student/Intern, Bahcesehir University, Faculty of Medicine, Istanbul,Turkey

3Medical Student/Intern, Bahcesehir University, Faculty of Medicine, Istanbul,Turkey

4Department of Neurosurgery, Neurosurgeon, Asoc Prof, Samsun Medicalpark Hospital, Samsun, Turkey

5Department of Pulmonary Medicine, MD, Pulmonologist, Samsun Medicalpark Hospital, Samsun, Turkey

6Department of Neurology, MD, Assistant, Ankara University,Faculty of Medicine, Ankara, Turkey

7Department of Pulmonary Medicine, MD, Assistant, Bashkir State Medical University, Faculty of Medicine,Ufa, Russia

*Corresponding author: Sevket Ozkaya, MD, Pulmonologist, Asoc. Prof., Bahcesehir University, Faculty of Medicine, Depart-ment of Pulmonary Medicine, Istanbul, Turkey; mobile phone: +90 532 474 13 09; E-mail: ozkayasevket@yahoo.com

Received Date: 01-08-2019 Accepted Date: 01-12-2019 Published Date: 03-18-2019 Copyright: © 2019 Sevket Ozkaya

Jacobs Journal of Pulmonology

AbstractNeurogenic pulmonary edema is a relatively rare and underdiagnosed clinical entitiy which is an increase in pulmonary in-terstitial and alveolar fluid. Neurogenic pulmonary edema develops within a few hours after a neurologic insult including spinal cord injury especially in subarachnoid hemorrhage. We aimed to present and discussion a 33-year-old man who developed neurogenic pulmonary edema following subarachnoid haemorrhage.

Keywords: Neurogenic pulmonary edema; subarachnoid haemorrhage; non-cardiogenic; pulmonary edema

Introduction

Neurogenic pulmonary edema(NPE) is a relatively rare and underdiagnosed clinical entitiy which is an increase in pulmonary interstitial and alveolar fluid. NPE develops within a few hours after a neurologic insult including spinal cord injury, subarachnoid hemorrhage(SAH), traumatic brain injury(TBI), intracranial hemorrhage, status epilepticus, menin-gitis, and subdural hemorrhage, have been associated with this syndrome(1-5). We aimed to present a patient who deve-loped NPE following subarachnoid haemorrhage.

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Case Presentation

A 33-year-old man with no history of any signifi-cant past medical illness, admitted to the emergency room sudden onset fainting and loss of consciousness. CT scan of the head revealed the massive subarachnoid blood which consistent with subarachnoid haemorrhage(Figure 1A and B).

Figure 1A: CT scan of the head showing the massive su-barachnoid blood which consistent with subarachnoid ha-emorrhage.

Figure 1B: CT scan of the head showing the massive su-barachnoid blood which consistent with subarachnoid ha-emorrhage.

Shortly after admission, respiratory failure was developed with tachypnea and tachycardia. He was intuba-ted and hemorrhagic pulmonary fluid was aspirated from endotracheal tube. Chest roentgenography showed the nonspecific, bilateral, rather homogeneous airspace con-solidative appearances with an apical predominance which supported the non-cardiogenic pulmonary edema(Figure 2).

Figure 2: Chest roentgenography showing the nonspecific, bilateral, rather homogeneous airspace consolidative appe-arances with an apical predominance which supported the non-cardiogenic pulmonary edema. Thoracic CT scans demonstrated the bilaterally dif-fuse alveolar edema which consistent with neurogenic pul-monary edema.(Figure 3 and 4).

Figure 3A.

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Figure 3B: The vertical section thoracic CT scans showing the bilaterally diffuse alveolar edema which consistent with neurogenic pulmonary edema(A and B).

Figure 4A.

Figure 4B: The coronal section thoracic CT scans showing the bilaterally diffuse alveolar edema(A and B). The pulmonary edema recovered after 24 hours of IV fluid and furosemid treatment(Figure 5).

Figure 5: Chest radiograhy showing to the recorvered pul-monary edema after the treatment.

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Discussion NPE is a potential early contributor to the pulmo-nary dysfunction. It develops within a few hours and caused by a myriad of CNS insults that raises Intracranial Pressu-re(ICP). Prevailing view is that a rapid elevation of ICP leads to neuronal compression , ischemia or damage ; followed by an autonomic response. Sympathetic nervous system activation leads to release of catecholamines that results in cardiopulmonary dysfunction. The cellular mechanisms that cause capillary leakage are also not well understood. Modifications in neurovegetative pathways are probably the cause of sudden, significant increases in microvascular pressure in the lungs, particularly in the pulmonary venules. This leads to reduced venous outflow, which in turn causes pulmonary capillary and arterial hypertension(7). Sudden onset of respiratory distress is a chief feature of NPE. Due to lack of treatment modalities , management of NPE consist of treating the underlying neurologic condition. Neurogenic pulmonary edema is described clinically as sudden onset breathlessness, tachypnoea, tachycardia, hemoptysis , bila-teral lung crackles on auscultation, low oxygen saturation on arterial blood gas analysis. Neurogenic pulmonary ede-ma seen as mostly homogenous, bilateral airspace consoli-dations(diffuse opacities) that predominate at the apices in about half of the cases, as seen in our case. Disappearance of radiologic findings in 1-2 days supports the absence of any diffuse alveolar damage(1-7) .In conclussion; NPE is acute onset and life-threatening com-plication especially in patients with subarachnoid hemor-rhage. If diagnosed immediately, the rapid response to tre-atment can be obtained.

Disclosure

“The authors have no conflicts of interest to declare”.

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